The medical term pulsus paradoxus refers to a quantifiable, exaggerated decrease in arterial blood pressure during inspiration. In normal patients, the decrease in arterial blood pressure during inspiration is in the range of about 2-5 mm Hg; whereas, in a patient suffering from certain medical conditions, pulsus paradoxus during inspiration may exceed this range and be on the order of 5-20 mm Hg or higher. Pulsus paradoxus has been noted in a variety of medical conditions including, but not limited to, asthma, croup, tension pneumothorax, pericardial tamponade, pulmonary embolus, hypovolemic shock, and sleep apnea.
The mechanisms of pulsus paradoxus are incompletely understood and may differ from disease process to disease process. In severe acute asthma, for example, large intrathoracic pressure variations are created by air trapping, causing a net increase in intraluminal airway pressure. The increased airway pressure is mechanically translated into increased intrapleural pressure, from a dramatically negative intrapleural pressure level during inspiration, to a positive intrapleural pressure level during expiration. Elevated intrathoracic pressure translates to increased impedance to right ventricular ejection which causes a markedly impaired left ventricular stroke output and concomitant reduction of left ventricular preload. These alterations contribute to paradoxic pulse in asthma and other respiratory and cardiovascular disease states.
Although measurement of pulsus paradoxus is recommended by authoritative medical practice guidelines (Steel et al., Acad Emerg Med 2:894-900 (1995); National Heart Lung and Blood Institute (NHLBI Guidelines for Emergency Department Asthma Management, NIH Publication, 1995), pulsus paradoxus is rarely recorded in clinical practice. Resistance by physicians to the application of pulsus paradoxus for the objective assessment of disease severity, asthma in particular, is largely due to the difficulty in measuring pulsus paradoxus in a rapidly breathing patient by methods known currently.
One conventional method for measuring pulsus paradoxus in a hospital emergency room setting is by the application of a sphygmomanometer, commonly referred to as a blood pressure cuff, that is cyclically inflated/deflated near a patient's systolic blood pressure. The operator determines systolic pressure during inspiration and expiration in separate maneuvers. This requires simultaneous observation of respiratory phase and cuff pressure. Typically, multiple operator efforts are required in order to arrive at a systolic pressure during inspiration and expiration. The objective is to determine how much the patient's blood pressure decreases during inspiration by bracketing the decrease in blood pressure within the cyclically varied cuff pressure. This process is ergonomically very difficult to perform and made even more so by the rapidly breathing patient. As a result, the method is inaccurate and interobserver results are excessively variable.
Despite problems inherent in this method of detecting pulsus paradoxus, the advantages of measuring and monitoring pulsus paradoxus are significant. A non-effort dependent, non-invasive measurement that provides immediate insight into how troubled is the act of breathing would be invaluable in the emergency room setting. The National Heart Lung and Blood Institute (NHLBI Guidelines for Emergency Department Asthma Management, NIH Publication, 1995) recognizes the advantages of measuring pulsus paradoxus and has recommended that pulsus paradoxus be measured on all asthmatic patients, despite inherent inaccuracies of the sphygmomanometric technique. Moreover, the NHLBI has advised that any patient with a pulsus paradoxus of 12 mm Hg or greater be hospitalized.
Common measures used currently to assess the severity of asthma are clinical assessment, arterial blood gas analysis, spirometry, and pulse oximetry; however, all are subject to certain shortcomings. Clinical assessment scores, for example, exhibit marked interobserver variability and have been incompletely validated. Arterial blood gas analysis is an invasive and painful technique and is often complicated by therapeutic administration of O.sub.2 and .beta.-adrenergic drugs and is therefore unreliable as an indicator of asthma severity. Tests of forced expiratory flow, as in spirometry, are effort dependent, typically cannot be used with children, and may actually exacerbate the underlying disease process.
Many experts are stymied to explain the rising mortality of asthmatic patients in view of the improving quality of acute pharmacological management of asthma and the enhanced sophistication of emergency physicians, as well as pre-hospital care systems. One explanation lies in the observation that there has been little change in how the asthmatic patient is evaluated acutely. A recent development in assessing acute asthma has been the use of pulse oximetry (SPO.sub.2) which measures the degree of oxygen saturation of hemoglobin non-invasively and empirically. Despite the unbiquitous availability of oximetry, .beta.-adrenergic drugs, used widely, may result in ventilation-perfusion shunts leading to a fall in SPO.sub.2 even though the patient is improving. It would appear that, SPO.sub.2, alone is an insensitive indicator of impending or continued respiratory distress.
A commonly used measure of asthmatic severity is peak flow rate (PFR) measurement. Despite widespread and long-standing use, PFR has been found to correlate poorly with asthma severity. This is not unexpected, given that a patient with a breathing impediment is asked to exhale as rapidly as possible against a fixed respiratory resistance. The best of three PFR values is typically used as a clinical measure. Subsequent measurements are taken to assess continually the severity of an asthmatic "attack" and how well the attack is resolving. Sudden death attributable to the necessary exertion required of an acutely asthmatic patient has been reported. Further, neither SPO.sub.2 nor PFR techniques can accurately determine whether a child needs to be admitted for asthma because PFR cannot be used in children less than 5 years of age and both measures have proven to be insensitive. SPO.sub.2 and PFR techniques correlate imperfectly with asthma severity.
New methods and devices are needed to reliably measure pulsus paradoxus. Surmounting the difficulties in measuring pulsus paradoxus will assist physicians in treating patients with pulsus paradoxus-associated diseases by quickly identifying those who are in more severe distress than apparent, from those who are rapidly responding to standard therapies. For example, in a prospective clinical study of 85 asthmatic children, it was reported that a pulsus paradoxus measurement of 11 mm Hg differentiated those children who needed hospitalization from those who did not (Wright et al., Arch. Ped. Adol. Med. 150:914-918 (1996)). An initial measurement of pulsus paradoxus may accurately determine the need for hospital admission among patients.